ArticleAmerican journal of physiology. Cell physiology2018
Transgelin induces dysfunction of fetal endothelial colony-forming cells from gestational diabetic pregnancies.
Article in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- A cell and transcriptome atlas of human arterial vasculature.Cell genomics · 2025Article
- The Acute Effects of Morning Bright Light on the Human White Adipose Tissue Transcriptome: Exploratory Post Hoc Analysis.Clocks & sleep · 2025Article
- Endothelial Progenitor Cells in Life, Pregnancy and Disease.Expert reviews in molecular medicine · 2025Review
- Generation of a novel constitutive smooth muscle cell-specific Myh11-driven Cre mouse model.Journal of molecular and cellular cardiology · 2025Article
- Bottom-up Biomaterial strategies for creating tailored stem cells in regenerative medicine.Frontiers in bioengineering and biotechnology · 2025Review
- Nanomedicine for Maternal and Fetal Health.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- Human Cord Blood Endothelial Progenitor Cells and Pregnancy Complications (Preeclampsia, Gestational Diabetes Mellitus, and Fetal Growth Restriction).International journal of molecular sciences · 2024Review
- Recent advances in endothelial colony-forming cells: from the transcriptomic perspective.Journal of translational medicine · 2024Review
- TGFJournal of diabetes research · 2024Article
- Enhancing endothelial colony-forming cells for treating diabetic vascular complications: challenges and clinical prospects.Frontiers in endocrinology · 2024Review
- The Effects of Preeclamptic Milieu on Cord Blood Derived Endothelial Colony-Forming Cells.bioRxiv : the preprint server for biology · 2023Article
- Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023Review
- Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023Review
- Impaired Angiogenic Function of Fetal Endothelial Progenitor Cells viaInternational journal of molecular sciences · 2023Article
- Synthetic hyaluronic acid coating preserves the phenotypes of lymphatic endothelial cells.Biomaterials science · 2023Article
- Engineering bioactive nanoparticles to rejuvenate vascular progenitor cells.Communications biology · 2022Article
- Neuropilin-1 deficiency in vascular smooth muscle cells is associated with hereditary hemorrhagic telangiectasia arteriovenous malformations.JCI insight · 2022Article
- RETRACTED: Tumor cell-secreted exosomal miR-22-3p inhibits transgelin and induces vascular abnormalization to promote tumor budding.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Cerebrospinal Fluid of Preeclamptic and Normotensive Pregnant Women Compared to Nonpregnant Women Analyzed with Mass Spectrometry.ACS omega · 2020Article
- Osteocyte Vegf-a contributes to myeloma-associated angiogenesis and is regulated by Fgf23.Scientific reports · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal exposure to gestational diabetes mellitus (GDM) predisposes children to future health complications including hypertension and cardiovascular disease. A key mechanism by which these complications occur is through the functional impairment of vascular progenitor cells, including endothelial colony-forming cells (ECFCs). Previously, we showed that fetal ECFCs exposed to GDM have decreased vasculogenic potential and altered gene expression. In this study, we evaluate whether transgelin (TAGLN), which is increased in GDM-exposed ECFCs, contributes to vasculogenic dysfunction. TAGLN is an actin-binding protein involved in the regulation of cytoskeletal rearrangement. We hypothesized that increased TAGLN expression in GDM-exposed fetal ECFCs decreases network formation by impairing cytoskeletal rearrangement resulting in reduced cell migration. To determine if TAGLN is required and/or sufficient to impair ECFC network formation, TAGLN was reduced and overexpressed in ECFCs from GDM and uncomplicated pregnancies, respectively. Decreasing TAGLN expression in GDM-exposed ECFCs improved network formation and stability as well as increased migration. In contrast, overexpressing TAGLN in ECFCs from uncomplicated pregnancies decreased network formation, network stability, migration, and alignment to laminar flow. Overall, these data suggest that increased TAGLN likely contributes to the vasculogenic dysfunction observed in GDM-exposed ECFCs, as it impairs ECFC migration, cell alignment, and network formation. Identifying the molecular mechanisms underlying fetal ECFC dysfunction following GDM exposure is key to ascertain mechanistically the basis for cardiovascular disease predisposition later in life.
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